UCLA’s AIDS (“Beetroot”) Institute discovers how HIV kills cells

HIV/AIDS vigilantes enjoyed many field days criticizing Thabo Mbeki’s health minister, cartooned as “Dr. Beetroot”, for suggesting the medical and nutritional value of a number of herbs and vegetables. Turns out that we have a Beetroot Institute right here in these medically scientific United States; moreover, funded by the HIV/AIDS mainstream:

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Herbal chemical helps combat HIV
LOS ANGELES, Jan. 1 (UPI) — Scientists at a Los Angeles multidisciplinary think tank say the herb Astragalus root may help fight HIV.
University of California, Los Angeles, AIDS Institute researchers say a chemical from the Chinese medicinal herb may help immune cells stave off the progressive loss of disease fighting ability caused by HIV, infections associated with chronic diseases or aging.
Immune cells are compromised as they age and their chromosomes — known as a telomere — become progressively shorter with cell division. The Astragalus root chemical prevents or at least slows down telomere shortening, the study said.
‘This has the potential to be either added to or possibly even replace the HAART — highly active anti-retroviral therapy — which is not tolerated well by some patients and is also costly,” study co-author Rita Effros said in a statement.
In a study published in the Journal of Immunology, Effros and colleagues show how the herbal plant chemical — called TAT2 — helped inhibit HIV replication.
“The ability to enhance telomerase activity and anti-viral functions of CD8 T-lymphocytes suggests that this strategy could be useful in treating HIV disease, as well as immunodeficiency and increased susceptibility to other viral infections associated with chronic diseases or aging,” the researchers said in a statement.
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AHA! HIV shortens telomeres! At last we know how HIV destroys the immune system!

Obviously it’s time to update Principles of Molecular Virology which still says:
“It is not clear how much of the pathology of AIDS is directly due to the virus and how much is caused by the immune system itself. There are numerous models which have been suggested to explain how HIV causes immune deficiency:
Direct Cell Killing: . . .
Antigenic Diversity: . . .
The Superantigen Theory: . . .
T-cell anergy: . . .
Apoptosis . . .
TH1-TH2 Switch: . . .
Virus Load and Replication Kinetics: . . .”

Henry Bauersaid

Another aspect that has long amused me is
“Primary Infection (or Acute Infection)
Primary HIV infection is the first stage of HIV disease, typically lasting only a week or two, when the virus first establishes itself in the body. Some researchers use the term acute HIV infection to describe the period of time between when a person is first infected with HIV and when antibodies (proteins made by the immune system in response to infection) against the virus are produced by the body (usually 6 to 12 weeks) and can be detected by an HIV test.”
This may be the only disease where “Acute Infection” is used to describe a phase where there are typically no symptoms, and the infectious agent can’t even be detected in any part of the body.

CathyVMsaid

Yes, Sepp, you are completely correct in your assertion.
“In cultured cells, AZT becomes preferentially incorporated into the DNA of chromosomal ends or telomeres, causing irreversible telomeric shortening and the potential for premature senescence [3, 11–13]. In experiments utilizing CHO cells exposed to 800 µM AZT for 24 hours were performed to obtain metaphase spreads that in turn were incubated with anti-AZT antibodies (Sigma, St Louis MO). A preferential localization of AZT within the telomeric region of the chromosomes was observed [14].”http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=18295533

Sabine Kalitzkussaid

Just imagine the case of a freshly hired employee (the virus!), who is nowhere detectable in the many offices of the company (the body) for a latency period of 10+ years. While enjoying this long latency period to engage in a variety of hobbies, the employee expects his bosses to “hit him hard and early” (i.e. from day one) by paying him life-extending monthly salaries in powerful doses, until he — possibly! — proceeds to behave like a full-blown employee, fulfilling his duties like, for example, supporting his bosses in creating better revenues.

But this thing is confusing me more and more. I just learned from Sepp’s blog, that there is not only one “HIV-disease”, there are many of them, though he does not tell us any specific numbers. He writes:

“Compare that alarmist data with the sober statistics given in mid-2006 by Statistics South Africa, which state that for 2000, HIV diseases numbered 10,321 or 2.5% of all deaths. In other words, even in 2007 Schneider and her associates retrospectively increased the number of HIV/AIDS deaths for 2000 in South Africa by 12 times! The data on death rates from “HIV diseases” from 1997 to 2004 in South Africa reveals other interesting anomalies from select provinces:

1) In 1997 in KwaZulu-Natal Province, “HIV diseases” accounted for 2.2% of all its deaths; in 2004, it was 2.3%.

2) In 1997 in Mpumalanga Province, “HIV diseases” accounted for 2.3% of all its deaths; in 2004 it was 2.2%.

3) In 1997 in Limpopo Province, “HIV diseases” accounted for 2.3% of all its deaths; in 2004, it was 2.0%.

4) In 1997 in Free State Province, “HIV diseases” accounted for 3.9% of all its deaths; in 2004, it was 2.1%.

5) And even for South Africa as a whole, in 1997 “HIV disease” was said to account for 2.0% of all deaths; in 2004 it had risen to 2.3%, but that was down from 2.6% in 1999.”

Nick Naylorsaid

What interests me is that with the exception of “Antigenic Diversity” and “Virus Load and Replication Kinetics”, mechanisms shown are consistent with what is now known about HERVs.

The exceptions represent the strongest legs of orthodoxy. The numbers produced by these models cannot be shown to relate to hard data (validation). Thus as you say elsewhere, “HIV” has no relation to “AIDS”. Case closed.